OBSERVATION

Reversal of Vision Metamorphopsia

Clinical and Anatomical Characteristics
Yaron River, MD; Tamir Ben Hur, MD, PhD; Israel Steiner, MD

Background: Metamorphopsia is a visual illusion that dis-
torts the size, shape, or inclination of objects. Reversal of
vision metamorphopsia (RVM) is a rare transient form of
metamorphopsia described as an upside-down, 180° rota-
tion of the visual field in the coronal plane. The patho-
physiological characteristics of RVM remain unclear.
Results: Five patients had parieto-occipital brain in-
sult sparing the primary visual cortex, and 3 also had evi-
dence of a concomitant brainstem or cerebellar syn-
drome. One patient had pure brainstem syndrome
underlying the RVM. Three patients had complete RVM
as well as oblique RVM of less than 180°.

Design: Patients with RVM had a complete neurologic
examination during or shortly after an episode of meta-
morphopsia, with particular emphasis on gaze disor-
ders, visual fields, visually guided hand movements, and
perceptual or cognitive deficits. Workup included im-
aging studies, visual field examinations, and brainstem
auditory and visual evoked response.
Setting: Department of Neurology, Hadassah Univer-
sity Hospital, Hebrew University-Hadassah Medical
School, Jerusalem, Israel.
Conclusions: These cases imply a possible anatomical
localization of the central integrator of visual extraper-
sonal orientation. Our observations suggest that a
separate central mechanism of visual orientation
might exist in each cerebral hemisphere and that
occipital and parietal lesions that spare the optic radia-
tions may account for the oblique and complete RVM.
We postulate that failure to perceive space in an allo-
centric coordinate frame, particularly in the coronal
roll plane, is potentially the critical event underlying
RVM.

Patients: Six consecutive patients were evaluated from

1991 to 1996. Arch Neurol. 1998;55:1362-1368

From the Department of
Neurology, Hadassah
University Hospital, Hebrew
University-Hadassah Medical
School, Jerusalem, Israel.
M
E T A M O R P H O P S I A is
characterized by an
optic illusion that al-
ters the size, shape, or
angulation of objects.
It is a rare manifestation of an acute cen-
tral nervous system insult, mainly to the
visual or vestibular systems.1 Reversal of
vision metamorphopsia (RVM) is a tran-
sient form of metamorphopsia described
as an upside-down, 180° alteration of the
visual field in the coronal plane.2 The first
case of RVM was reported by Winslow3 in
1868 as a transient phenomenon of hys-
teria. The transient nature of this phenom-
enon was clearly evident in this early re-
port as well as in subsequent cases. Only
rarely was it observed as a stable phenom-
enon lasting days or weeks.4 Klopp5 re-
viewed the German literature and added
3 of his RVM cases. He was able to find
13 patients with this disorder: 2 had non-
organic or psychogenic disturbance, 5 had
cortical (mainly parietal) lesions, 4 had
brainstem lesions, and 2 had cerebellar le-
sions. The causes of RVM are diverse, in-
cluding head trauma, tumors, and stroke.
Klopp5 suggested that RVM is not caused
by an insult to the optic pathways but
rather by a central nervous system distur-
bance of the vestibular system affecting the
perception of the body in space or the per-
ception of the subjective visual vertical.
For editorial comment
see page 1285
The most thorough review of RVM is
by Solms et al,6 who analyzed 21 cases.
They conclude that RVM is a transient,
sudden, and paroxysmal phenomenon. It
is perceived as an actual torsion of the vi-
sual array with 180° rotation in the coro-
nal plane, usually in a clockwise direc-
tion. Tilting of the visual field less then
180° (for example, 90°) in the coronal

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 plane or RVM of the sagittal and horizontal planes is as-
sociated with common coronal RVM in some of the cases
reviewed by Solms et al. Vertigo and malaise are com-
mon, but distorted egocentric orientation (ie, the pa-
tient experiences standing on his head or feels that his
body is tilted away from the vertical7,8) is rare.6
In the last 5 years, we have observed 6 patients with
RVM. Our evaluation of these cases has contributed to
our understanding of this disorder.
REPORT OF CASES
CASE 1
A 60-year-old patient was admitted to the emergency
department reporting that he suddenly heard a “loud
voice” immediately followed by dizziness and weakness
in his right hand. His medical history included hyper-
tension, hypercholesterolemia, type 2 diabetes mellitus,
and ischemic heart disease. On examination, the
patient’s blood pressure was 160/100 mm Hg and his
pulse was 60/min and regular. Findings from a general
physical examination were normal. Neurologic exami-
nation revealed a conscious, fully alert, and mentally
intact patient with right-sided dysmetria, gait ataxia
with a tendency to fall to the right, and a horizontal
rotatory nystagmus on right lateral gaze. A vertical nys-
tagmus was observed on gazing upward. Eight hours
after the appearance of dizziness and weakness in the
right hand, the patient experienced a visual distur-
bance. The objects in his right visual field appeared
upside down. People were seen walking on their heads,
the windows close to the ceiling were within reach of
his hands, and a cup stood “upside down” on the shelf
but the “tea did not spill out” (all the objects including
the shelf were upside down). In his left visual field, the
patient perceived objects as tilted in a counterclockwise
direction (45°-90°, Figure 1). The visual symptoms
lasted for 3 hours and then remitted spontaneously.
After remission, results from a visual field examination
were normal. Findings from a brain computed tomo-
graphic scan, an electroencephalogram, and a cerebro-
spinal fluid examination were within normal limits.
Bilateral visual evoked potential recordings showed
normal configuration and latency of the P100 wave.
Brainstem auditory response was normal on the left side
and pathologic on the right, with a first to fifth inter-
wave latency of 6.1 milliseconds (reference range, #4.6
milliseconds). Results from a perimetric visual field
evaluation were normal. Magnetic resonance imaging
performed 6 days after the episode demonstrated
infarcts of both occipital lobes (Figure 2) occupying
an area anterior to the striate cortex in the periphery of
Brodmann areas 17 and 18. The infarct on the left was
larger. In addition, right cerebellar and middle cerebel-
lar peduncle infarcts were present (Figure 3).
CASE 2
A 70-year-old patient with hypertension and diabetes
had an episode of true vertigo 1 month before admis-
sion for repeated episodes of vertigo and instability of
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R
LR L
A
LR
LR
LR
B
LR
LR
C
LR
LR
D
LR RL
E
Figure 1. The asymmetrical letters R in the right visual field and L in the left
visual field are used to demonstrate the reversal of vision phenomenon.
A, Reversal of vision in patient 1. Note the counterclockwise tilting of the left
visual field and complete 180° reversal of vision of the right visual field.
B, Reversal of vision in patient 4. Complete reversal of vision was interrupted
by oblique clockwise vision metamorphopsia. C, Complete reversal of vision
in the coronary plane in patients 2, 3, 5, and 6. D, Complete reversal of vision
in the sagittal plane. E, Complete reversal of vision in the horizontal plane.
gait. Findings from a neurologic examination showed
left cerebellar syndrome, left horizontal nystagmus, and
a transient absence of the right optokinetic nystagmus.
The patient’s visual fields were normal. Two hours after
the vertiginous attack, he had a complete RVM that
lasted for approximately half an hour (Figure 1, C). The
RVM momentarily disappeared when the patient saw
the flame of a match or his hand moving in front of
him. A computed tomographic scan demonstrated bilat-
eral occipital stroke occupying Brodmann area 18
(Figure 4).
CASE 3
A 79-year-old patient with hypertension was admitted
because of acute vertigo. On examination, bilateral cer-
ebellar and pyramidal tract signs were observed but the
patient was neurologically stable. Results from a com-
puted tomographic scan were normal. A few hours after
admission, the acute episode of vertigo disappeared but
the patient developed a sensation of body levitation fol-
lowed by a counterclockwise rotation of his visual
fields. Within 10 minutes, he experienced a complete
RVM. He saw people walking on their heads, and the
 Figure 2. Axial T2-weighted magnetic resonance imaging scan (repetition
time, 2200 milliseconds; echo time, 80 milliseconds) through the occipital
regions of patient 1 demonstrating fresh infarcts of both occipital lobes,
Brodmann areas 17 and 18, which spare the occipital poles (arrows). The
assignment of the lesions was based on the study by Damasio and
Damasio.27
floor next to his bed appeared to be over his head. To
the patient’s embarrassment, he made the wrong hand
movements when he tried to cover himself with the
blanket or to pick up a cup of tea. On examination
shortly after the episode of metamorphopsia had disap-
peared, gaze apraxia with preserved oculocephalic
reflexes to all directions was noted. In addition, the
patient had optic ataxia without simultanagnosia. When
presented with an object in his right upper visual field,
he directed his hands to his lower left hemispace. The
patient correctly identified the chirality of hands pre-
sented to him. His condition stabilized, and results
from a repeated neurologic examination the next day
were normal aside from bilateral pyramidal tract signs
and a mild gait ataxia. The clinical course and the neu-
rologic findings suggested a vertebrobasilar stroke and a
transient ischemic attack of the posterior circulation
affecting the parietal lobes.
CASE 4
A 56-year-old woman had 4 years of recurrent epi-
sodes of true vertigo, near syncope, speech distur-
bances, and inability to control her right hand. These
episodes lasted for approximately an hour and some-
times were followed by severe occipital pain or hemi-
crania. Several episodes were accompanied by a sensa-
tion of “heaviness” in her face and dysphagia. During
1 of the episodes, severe vertigo with weakness in the
right hand and an inclination of the body to the right
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Figure 3. Axial T2-weighted magnetic resonance imaging scan (repetition
time, 2200 milliseconds; echo time, 80 milliseconds) through the superior
cerebellar regions of patient 1 demonstrating fresh infarct of the right
superior cerebellar region and middle cerebellar peduncle. The dark
hypodense regions in the right cerebellar and left occipital infarcts represent
acute hemorrhage.
were accompanied by complete RVM that lasted 45
minutes and was interrupted by oblique clockwise-
vision metamorphopsia (Figure 1, B). A repeated epi-
sode of oblique vision occurred a few months later and
was associated with tilting of vision in the sagittal
plane of less than 90°. The patient was admitted for an
examination, the results of which revealed blood pres-
sure of 120/80 mm Hg and a regular pulse of 88/min.
Findings from a general physical and neurologic
examination were normal apart from mild dysmetria
on the right upper and lower extremities and upward
vertical nystagmus. Results from a laboratory investi-
gation revealed hypothyroidism and hyperlipidemia.
The patient’s cerebrospinal fluid was normal without
oligoclonal bands. There was no serologic evidence of
a collagen vascular disease. Findings from an electro-
encephalogram and audiometry were normal. A brain-
stem evoked response study showed bilateral prolon-
gation of the first to fifth interwave latency (.6
milliseconds; reference range,,5 milliseconds). T 2-
weighted magnetic resonance imaging demonstrated
4 small hyperintense foci in the white matter above
and below the tentorium, which were compatible with
the patient’s age. Since the patient had experienced
severe headaches during some of the episodes, a tenta-
tive diagnosis of basilar migraine was made and treat-
ment with propranolol hydrochloride was started
at 160 mg/d. A dramatic improvement in both the se-
verity and frequency of the episodes ensued. Also of
note was the considerable reduction in some of the

Figure 4. Axial computed tomographic scan without contrast demonstrating
bilateral hypodense occipital regions occupying Brodmann area 18.27
acute attacks following treatment with sumatriptan
succinate.
CASE 5
A 54-year-old patient was admitted because of recur-
rent seizures. His medical history included severe ische-
mic heart disease and angina pectoris, diabetes mellitus
with diabetic retinopathy and neuropathy, and periph-
eral vascular disease. A right hemispheric cerebrovascu-
lar accident had caused a left hemihypoesthesia 10 years
before his present admission. Two weeks before admis-
sion, the patient had episodes of confusion, delusions,
and visual hallucinosis, with the experience that some-
body was nearby when he was alone. In addition, the pa-
tient experienced recurrent twitching of the left side of
his face. On the day of his admission, the patient expe-
rienced multiple adverse seizures with deviation of the
eyes and head to the left and tonic convulsions of the left
hand. He reported seeing a stereotypic visual aura: a dark
tunnel ending with a bright flash of light. On 3 occa-
sions, the patient had complete RVM postictally, which
lasted for approximately 5 to 10 minutes, during which
he was fully oriented and not confused (Figure 1, C). Find-
ings from a neurologic examination revealed mild left
hemihypoesthesia and hemiparesis, hypometric sac-
cades to the left, disturbed eye pursuit movements to the
right, disturbed left optokinetic nystagmus, and tran-
sient left hemianopia. A few hours later, the patient’s ocu-
lar and visual disturbance disappeared, but left hemipa-
resis and hemihypoesthesia persisted. Results from a
computed tomographic scan with contrast material dem-
onstrated right parietal enhancement.
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Results from an electroencephalogram performed a
few minutes after the disappearance of metamorphop-
sia showed slow theta and delta background activity with
focal epileptiform activity in the right parietal and pos-
terior temporal regions. The patient was treated with con-
tinuous intravenous diazepam and the seizures ceased
within 48 hours.
CASE 6
A 75-year-old patient who was a heavy smoker with
chronic obstructive lung disease and ischemic heart dis-
ease was involved in a car crash. He sustained polytrauma,
including brain concussion and laceration of the scalp.
Results from a computed tomographic scan showed a left
temporo-occipital linear skull fracture without paren-
chymal brain injury. The morning after the crash, the pa-
tient woke up and saw people around him walking on
their heads, his entire visual field turned completely up-
side down. This phenomenon lasted for approximately
half an hour and recurred 48 hours later for a short pe-
riod. Findings from a neurologic examination after the
second episode of metamorphopsia were normal. Nei-
ther ocular motility abnormality nor cerebellar dysfunc-
tion were observed.
COMMENT
Thirty cases of RVM have been reported in the litera-
ture.3-21 A critical analysis of these cases and our own ob-
servations allow us to draw certain conclusions regard-
ing the clinical and pathophysiological aspects of this
phenomenon.
Reversal of vision was a transient phenomenon in
all of our patients. It involved the rotation of the entire
visual array without distorting other features of the
extrapersonal space. Body sense disturbances with
inclination or levitation of the body occurred in 3
patients (cases 1, 3, and 4), but was relatively mild
when metamorphopsia occurred. In addition, none of
the patients experienced a complete reversal of their
bodies in space (ie, no patients had nonvisual percep-
tions of walking on their heads). Only 5 patients
(16%) described in the literature had dramatic alter-
ations in body sense, such as body tilt, a sense of com-
plete body reversal, or head tilt. 5,7,8,13,20 All except
Halpern’s 7 patient had an insult to the brainstem.
These findings suggest that RVM is primarily a visual
illusion of the extrapersonal space, and that the alter-
ation of the body scheme is the result of a dysfunction
of vestibular centers in the brainstem. Alternatively,
body scheme disorders could be epiphenomenona.
This conclusion is supported by the early experiments
of Stratton,22 who used goggles that reinverted the reti-
nal image. The visual scene was inverted in the coro-
nal (upside down) and horizontal (right to left)
planes. Consequently, one’s sense of body parts and
whole body position was acutely altered.
Transient recovery from metamorphopsia occurred
in 1 of our patients (case 2) when he moved his hand in
front of him or in response to a familiar visual object
with a certain orientation. This is an important observa-
 Patients With Reversal of Vision Metamorphopsia (RVM)*
Patient No./ Duration of RVM
Age, y/Sex Cause (No. of Episodes)
1/60/M Bilateral occipital and 3h
cerebellar CVA
2/70/M Vertebrobasilar TIA 30 min
3/79/M Brainstem CVA 10 min
4/56/F Basilar migraine 45 min (3)
5/54/M Complex partial seizure 5-10 min (3)
6/75/M Brain concussion and 30 min (2)
left occipitotemporal
fracture
*CVA indicates cerebrovascular accident; IHD, ischemic heart disease; TIA, transient ischemic attack; DM, diabetes mellitus; OKN, optokinetic nystagmus; and
NA, not applicable.
tion because it shows that certain stimuli can correct
and reinvert the visual scene. A functional dissociation
exists in the human brain of near and far visual space
perception. The movement of a hand in the periper-
sonal space might activate neuronal networks with peri-
cutaneous receptive fields.23 These networks, which
process information from the peripersonal space, might
correct RVM, which is primarily brought about by
lesions to networks related to far space perception.
Four patients described in the literature had transient
recoveries from RVM usually in response to eye closure
or changes in body position.5,6,14,15 Polysensory neurons
that respond to visual stimuli and are selective to the
spatial characteristics of hand movements24 and neu-
rons that respond to visual and somatosensory stimuli
in area 7b25 might also be involved in the process of
recovery. Stratton 22 showed that after a few days of
wearing goggles that inverted the retinal image, subjects
could realign and reinvert the visual scene without tak-
ing off the goggles. This demonstrates the enormous
plasticity of the specific neuronal networks involved in
spatial frame perception.
None of the patients in our series had visual field
defects at the time of the RVM. Only 1 patient (case 5)
had transient hemianopsia before metamorphopsia
occurred, which is consistent with an early observation
of Critchley,26 who pointed out that metamorphopsia
occurs when lesions approximate the visual cortex and
the geniculostriate radiations but do not actually
involve them.
It was difficult and at times impossible to deter-
mine the geometrical relationship of rotations and
reflections of the visual world to chirality in our
patients and those described in the literature. Meta-
morphopsia was reported along each of the principal
orthogonals, although it was rare in the sagittal and
horizontal planes.5,7,11,15 The most common distortion
is a rotation along the coronal plane, which flips the
top and bottom and the left side of objects to the right
and vice versa, but keeps a left hand looking like a left
hand appearing in the contralateral part of the space
(Figure 1, C). In contrast, an inversion along the sagit-
tal plane would result in a top-bottom mirror reflec-
©1998 American Medical Association. All rights reserved.
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Signs and Symptoms Associated Disease Ocular Motility Disorder
Right cerebellar syndrome Hypertension and IHD Right horizontal and rotatory nystagmus
Left cerebellar syndrome Hypertension and DM Left horizontal nystagmus and
decreased right OKN
Optic ataxia and gaze apraxia Hypertension Gaze apraxia
Right clumsy hand Hyperlipidemia and Vertical nystagmus
hypothyroidism
Transient left hemianopia and Hyperlipidemia, DM, Disturbed pursuit eye movements
left hemihypoesthesia and IHD
NA NA NA
tion, making a left hand look like a right hand.
Although chirality is inverted, a left hand would stay
in the left visual field (Figure 1, D). One patient (case
4) described an incomplete (,180°) inversion of the
visual field in the sagittal plane. Horizontal-plane
metamorphopsia would not bring about a top-bottom
RVM but a right-left reversal, such that a right hand
would appear to be a left hand in the wrong (contra-
lateral) part of space (Figure 1, E).
Three patients had oblique vision, 1 with clock-
wise and 2 with counterclockwise rotation of the visual
field (cases 1 and 4 [Figure 1, A and B], and 3). This phe-
nomenon accompanying RVM was reported in 5 cases
in the literature.5,7,8,10,12 In these cases, the visual scene
was tilted less than 180°. Case 1 in our study is particu-
larly interesting in this regard. This patient had asym-
metrical bilateral stroke in Brodmann areas 17 and 18.
Consequently, the patient experienced both RVM and
counterclockwise tilting of vision simultaneously in dif-
ferent parts of his visual field. This might indicate that
both phenomena are interrelated and that a separate cen-
tral integrator of visuospatial orientation exists in each
hemispheric visual cortex, possibly within the posterior
parietal and occipital areas.
One patient (case 3) had RVM in the coronal plane
with a reaching disorder. Apparently, he executed con-
tralateral reaching movements that correspond to Fig-
ure 1, C. He did not have self right to left confusion, and
he was able to identify the chirality of hands presented
to him. We did not observe right to left confusion in our
patients, suggesting that this phenomenon is not re-
lated to RVM.
In all patients, vomiting, dizziness, and feelings of
malaise were reported. Ocular motility disorder was found
in 5 of 6 of our patients (Table ). This condition has been
recognized in many other patients,5,8,14,19-21 but its patho-
physiological significance remains unclear.
Five of our patients (cases 1-3, 5, and 6) had signs
and/or results from imaging studies or electrophysi-
ological studies consistent with occipital or parieto-
occipital lesions. A stroke in the occipital region, Brod-
mann area 18, was found in 2 patients (cases 1 and 2,
according to the Damasio plates27). Brainstem auditory
ARCH NEUROL / VOL 55, OCT 1998
1366
 evoked response was unilaterally or bilaterally abnor-
mal in 2 patients (cases 1 and 4). Four patients had ver-
tigo, cerebellar signs, or even brainstem cerebrovascular
accident prior to metamorphopsia (cases 1-4). One
patient (case 3) had signs of Balint syndrome. Although
most of our patients had a cortical parieto-occipital syn-
drome, such conditions were not reflected in previous
cases. When the site of the insult was documented in
patients with RVM, it was found to involve 2 main
regions, the parieto-occipital region and the brainstem.6
If we include our patients, 7 (16%) of 36 patients (30
previous cases and our own 6 patients) had a brainstem
lesion.17,19,20,22 Three patients had a medullary insult,8,13
4 had a cerebellar lesion,12,14,19,20 and 7 had a parieto-
occipital lesion.7,9,11,15 One patient had an unusual fron-
tal lesion6 (in addition to the case of Halpern7 with cys-
ticercosis involving mostly the parieto-occipital region
but also the frontal lobes). One patient (case 3) had
transient vertebrobasilar ischemic attacks with brain-
stem and occipital lobe syndrome.21
Thus, 15 (41%) of 36 patients described in the lit-
erature had infratentorial lesions, whereas only 8 pa-
tients (22%) had parieto-occipital lesions. However, in
many of the cases with brainstem syndromes, the cause
was either a vertebrobasilar transient ischemic attack or
a cerebrovascular accident. It is plausible that the actual
phenomenon of RVM in patients with brainstem syn-
dromes occurred when ischemia affected the parieto-
occipital area rather than brainstem structures. Most of
the cases of RVM were reported before the era of mod-
ern imaging. Therefore, it is conceivable that some of the
patients with brainstem syndromes had concomitant pa-
rieto-occipital lesions.
What are the mechanisms underlying RVM? The
spatial representation of visual stimuli in the central
nervous system is formed by combining information
from various modalities, both retinal and extraretinal.
To create a valid representation of space, a series of
coordinate frame transformations is performed. Retinal
inflow is combined with ocular position information to
produce head-centered representation.28-30 To represent
body-centered coordinates, the 7a parietal cortex and
the intraparietal area have neurons that respond to the
eye position as well as the head position.30 The relation-
ship between the relevant representation of visual
stimuli and RVM is based on world-centered coordi-
nates (allocentric). Information about the position of
the head derives from otolith and vestibular inputs
together with proprioceptive information from neck
muscles. These signals, when combined with eye and
retinal position information, can encode locations in
world-based coordinates.30,31 Experiments in rats typi-
fied “direction tuned” cells, the activity of which were
modulated by the orientation of the whole body. These
cells in the posterior parietal region are multimodal
cells. They are activated by both visual and integral ves-
tibular signals to form the representation of space.30,32
We know that this orientation system is widely distrib-
uted in the central nervous system.30 This might explain
the various locations of insults causing RVM. It is clear
that both retinal and extraretinal disturbances can bring
about a mismatch of information that would lead to
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RVM. Any transient inconsistent correspondence of
vestibular information or lack of information due to a
brainstem lesion would potentially lead to RVM. In
particular, a disturbance of the central otolith pathway
that would deprive higher brain centers of necessary
information about the head position in the roll plane,
which is the plane relevant to the phenomenon of
RVM in most patients. Distinct areas in the brainstem
that mediate vestibular tone in the horizontal, vertical,
and roll planes have recently been discovered.33 Dys-
function of these specific regions in the brainstem
might lead to vestibular tone imbalance, and that in
turn would induce RVM along 1 or more of the princi-
pal orthogonals.
In conclusion, failure to perceive space in an allo-
centric coordinate frame, particularly in the coronal
roll plane, is potentially the critical event underlying
RVM. Reversal of vision is always a transient visual
illusion caused by either brainstem or parieto-occipital
lesions. It is a pure disorder of far space perception
that should be clearly differentiated from certain body
scheme disorders and other types of visual meta-
morphopsia. The polymodal nature of the neuronal
network that governs the perception of allocentric
coordinates and their widespread distribution in the
central nervous system might allow for a rapid recov-
ery from RVM when correct and new information is
processed.
Accepted for publication March 23, 1998.
This work was supported in part by the Sol Irwin Juni
Memorial Fund and the Hilda Katz Blaustein Fund, Jerusa-
lem, Israel.
We would like to thank Jane Loitman, MD, for criti-
cally reviewing the manuscript, and Izchak River, MS, for
helping with the translation of the non-English articles.
Reprints: Yaron River, MD, Department of Neurol-
ogy, Hadassah University Hospital, Hebrew University-
Hadassah Medical School, PO Box 12000, Jerusalem 91120,
Israel.
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